Dendritic cells do not transduce inflammatory stimuli via the capsaicin receptor TRPV1

被引:33
作者
O'Connell, PJ
Pingle, SC
Ahern, GP
机构
[1] Robarts Res Inst, London, ON N6A 5K8, Canada
[2] Univ Western Ontario, Dept Surg, London, ON N6A 3K7, Canada
[3] Univ Western Ontario, Dept Microbiol & Immunol, London, ON N6A 3K7, Canada
[4] Georgetown Univ, Dept Pharmacol, Washington, DC 20007 USA
关键词
dendritic cells; transient receptor potential channel vanilloid type 1; vanilloid receptor 1; capsaicin; inflammation; substance;
D O I
10.1016/j.febslet.2005.08.023
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Inflammatory stimuli provide critical activation signals for dendritic cells (DC). Signaling through the capsaicin receptor TRPV1 is reported to initiate DC maturation and migration. We attempted to characterize TRPV1 channels in DC. Capsaicin or extracellular protons failed to elicit a change in intracellular [Ca2+] or membrane current in DC. In contrast, capsaicin evoked a sustained increase in [Ca2+] and large inwards currents in sensory neurons and TRPV1-expressing HEK293 cells. TRPV1 expression was confirmed by RT-PCR in sensory neurons, but was undetectable in DC. Interestingly, and in contrast to capsaicin, the inflammatory neuropeptide substance P evoked Ca2+ transients in DC. Thus, our data do not support the hypothesis that DC express TRPV1 channels. Rather, signaling through TRPV1 in sensory nerves may modulate DC via neurogenic actions. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:5135 / 5139
页数:5
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